Immunohistochemical study of the distribution of neuronal voltage-gated calcium channels in the nNOS knock-out mouse cerebellum

Nitric oxide (NO) participates in synaptic plasticity, neuronal development, and apoptosis. The involvement of NO and ionic calcium in synaptic plasticity imply that NO may exert an effect on Ca ²⁺ channels. Therefore, we investigated changes in the expressions of calcium channel subunits (Ca _v1.2/α _1C, Ca _v1.3/ α _1D, Ca _v2.1/α _1A, and Ca _v2.2/α _1B) in nNOS knock-out (-/-) (nNOS ^(-/-)) mouse cerebellum using an immunohistochemical approach. We found that the immunoreactivities of the Ca _v1.2 and Ca _v1.3 subunits were reduced in the cell bodies of Purkinje cells in these mice and that the signal of the Ca _v1.2 subunit in neurons and of the Ca _v1.3 subunit in the neuropils of nNOS ^(-/-) mice cerebellar nuclei were significantly down-regulated. We show, for the first time, that prolonged NO deficiency in the cerebellum may affect calcium channel protein expressions, especially, of the Ca _v1.2 and Ca _v1.3 subunits.